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本文引用的文献

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Human alveolar macrophage responses to air pollution particulates are associated with insoluble components of coarse material, including particulate endotoxin.人类肺泡巨噬细胞对空气污染颗粒物的反应与粗颗粒物质的不溶性成分有关,包括颗粒内毒素。
Toxicol Appl Pharmacol. 2001 Feb 15;171(1):20-6. doi: 10.1006/taap.2000.9096.
2
Enhancement of allergic inflammation by diesel exhaust particles: permissive role of reactive oxygen species.柴油尾气颗粒增强过敏性炎症:活性氧的促进作用。
Ann Allergy Asthma Immunol. 1999 Dec;83(6 Pt 2):624-9. doi: 10.1016/S1081-1206(10)62884-0.
3
Fine particles are more strongly associated than coarse particles with acute respiratory health effects in schoolchildren.在学童中,细颗粒物比粗颗粒物与急性呼吸道健康影响的关联更强。
Epidemiology. 2000 Jan;11(1):6-10. doi: 10.1097/00001648-200001000-00004.
4
Cytotoxicity and induction of proinflammatory cytokines from human monocytes exposed to fine (PM2.5) and coarse particles (PM10-2.5) in outdoor and indoor air.暴露于室外和室内空气中的细颗粒物(PM2.5)和粗颗粒物(PM10 - 2.5)后,人单核细胞的细胞毒性及促炎细胞因子的诱导情况。
Toxicol Appl Pharmacol. 1999 Mar 15;155(3):245-52. doi: 10.1006/taap.1998.8591.
5
Acute inflammatory responses in the airways and peripheral blood after short-term exposure to diesel exhaust in healthy human volunteers.健康人类志愿者短期接触柴油废气后气道和外周血中的急性炎症反应。
Am J Respir Crit Care Med. 1999 Mar;159(3):702-9. doi: 10.1164/ajrccm.159.3.9709083.
6
Decreased CD11b expression, phagocytosis, and oxidative burst in urban particulate pollution-exposed human monocytes and alveolar macrophages.暴露于城市颗粒物污染的人类单核细胞和肺泡巨噬细胞中CD11b表达、吞噬作用及氧化爆发降低。
J Toxicol Environ Health A. 1998 Dec 11;55(7):455-77. doi: 10.1080/009841098158278.
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Urban particle-induced apoptosis and phenotype shifts in human alveolar macrophages.城市颗粒物诱导人肺泡巨噬细胞凋亡及表型转变
Environ Health Perspect. 1998 Mar;106(3):127-32. doi: 10.1289/ehp.98106127.
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The effect of cigarette smoking on the bone marrow.吸烟对骨髓的影响。
Am J Respir Crit Care Med. 1997 Mar;155(3):1021-6. doi: 10.1164/ajrccm.155.3.9116981.
9
Is daily mortality associated specifically with fine particles?每日死亡率是否与细颗粒物有特定关联?
J Air Waste Manag Assoc. 1996 Oct;46(10):927-39.
10
Enhanced human IgE production results from exposure to the aromatic hydrocarbons from diesel exhaust: direct effects on B-cell IgE production.接触柴油废气中的芳烃会导致人类IgE产生增加:对B细胞IgE产生的直接影响。
J Allergy Clin Immunol. 1995 Jan;95(1 Pt 1):103-15. doi: 10.1016/s0091-6749(95)70158-3.

吸入细颗粒物(PM2.5)不会调节正常人类受试者血液或肺部的宿主防御或免疫参数。

Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.

作者信息

Harder S D, Soukup J M, Ghio A J, Devlin R B, Becker S

机构信息

National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA.

出版信息

Environ Health Perspect. 2001 Aug;109 Suppl 4(Suppl 4):599-604. doi: 10.1289/ehp.01109s4599.

DOI:10.1289/ehp.01109s4599
PMID:11544170
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1240588/
Abstract

We tested the hypothesis that exposure of healthy volunteers to concentrated ambient air particles (CAPS) between 0.1 and 2.5 microm in diameter is associated with modulation of human alveolar macrophage (AM) function, cytokine production, and immune phenotype in both blood and lung. Thirty-eight volunteers were exposed to either filtered air or CAPS from the immediate environment of the U.S. Environmental Protection Agency human studies facility in Chapel Hill, North Carolina, USA. Particle concentrations in the chamber during the exposures ranged from 23.1 to 311.1 microg/m3. No symptoms were noted by volunteers after the exposure. Eighteen hours after exposure, analysis of cells obtained by bronchoalveolar lavage (BAL) showed a mild increase in neutrophils in both the bronchial (8.4 +/- 2%) and alveolar fractions (4.2 +/- 1.7%) in subjects exposed to the highest concentration of CAPS compared to neutrophils in the fluids of those exposed to filtered air (bronchial fraction 2.7 +/- 0.6%; alveolar fraction 0.8 +/- 0.3%). There was no change in the percentage of lymphocytes or AMs recovered in the lavage after inhalation of the highest particle levels (mean 207 microg/m3). There was also no change in the proportion of lymphocytes in the BAL expressing CD3, CD4, CD8, CD19, nor activation markers CD25 or CD69. Particle inhalation did not affect the expression of CD11b, CD64, CD16, CD14, CD71 on AM, nor was there an effect on phagocytosis or oxidant generation following stimulation with zymosan A. IL-6 and IL-8 levels detected by enzyme-linked immunoabsorbent assay in the BAL were unrelated to inhaled particle levels. The distribution of lymphocyte subsets in blood obtained 18 hr after exposure to CAPS did not differ from that found before exposure. We conclude that ambient air particles are capable of inducing a mild inflammation in the lower respiratory tract but have no effect on immune phenotype or macrophage function under the conditions tested.

摘要

我们验证了以下假设

让健康志愿者暴露于直径在0.1至2.5微米之间的浓缩环境空气颗粒物(CAPS)中,会对人体肺泡巨噬细胞(AM)功能、细胞因子产生以及血液和肺部的免疫表型产生调节作用。38名志愿者被暴露于来自美国北卡罗来纳州教堂山的美国环境保护局人体研究设施附近环境的过滤空气或CAPS中。暴露期间室内的颗粒物浓度范围为23.1至311.1微克/立方米。暴露后志愿者未出现任何症状。暴露18小时后,对通过支气管肺泡灌洗(BAL)获得的细胞进行分析,结果显示,与暴露于过滤空气的受试者(支气管部分为2.7±0.6%;肺泡部分为0.8±0.3%)的灌洗液中的中性粒细胞相比,暴露于最高浓度CAPS的受试者的支气管(8.4±2%)和肺泡部分(4.2±1.7%)中的中性粒细胞略有增加。吸入最高颗粒物水平(平均207微克/立方米)后,灌洗回收的淋巴细胞或AM的百分比没有变化。BAL中表达CD3、CD4、CD8、CD19的淋巴细胞比例以及激活标志物CD25或CD69也没有变化。吸入颗粒物并未影响AM上CD11b、CD64、CD16、CD14、CD71的表达,用酵母聚糖A刺激后对吞噬作用或氧化剂生成也没有影响。通过酶联免疫吸附测定法在BAL中检测到的IL-6和IL-8水平与吸入的颗粒物水平无关。暴露于CAPS 18小时后采集的血液中淋巴细胞亚群的分布与暴露前没有差异。我们得出结论,在测试条件下,环境空气颗粒物能够在呼吸道下部诱发轻度炎症,但对免疫表型或巨噬细胞功能没有影响。